Title : Mutual exclusivity analysis of genetic and epigenetic drivers in melanoma identifies a link between p14 ARF and RARĪ² signaling.

Pub. Date : 2013 Oct

PMID : 23851445






3 Functional Relationships(s)
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1 Mechanistically, all-trans retinoic acid (ATRA) treatment increased the expression of p14(ARF) in primary human melanocytes and the steady-state levels of p14(ARF) in these cells were shown to be regulated via RARbeta. Tretinoin retinoic acid receptor beta Homo sapiens
2 Mechanistically, all-trans retinoic acid (ATRA) treatment increased the expression of p14(ARF) in primary human melanocytes and the steady-state levels of p14(ARF) in these cells were shown to be regulated via RARbeta. Tretinoin retinoic acid receptor beta Homo sapiens
3 Furthermore, the ability of ATRA to induce senescence is reduced in p14(ARF)-depleted melanocytes, and we provide proof-of-concept that ATRA can induce irreversible growth arrest in melanoma cells with an intact RARbeta-p14(ARF) signaling axis, independent of p16(INK4A) and p53 status. Tretinoin retinoic acid receptor beta Homo sapiens